Amir Tirosh, MD, PhD; Assaf Rudich, MD, PhD; Tzippora Shochat, MSc; Dorit Tekes-Manova, MD; Eran Israeli, MD; Yaakov Henkin, MD; Ilan Kochba, MD; Iris Shai, RD, PhD
Note: Drs. Tirosh and Rudich contributed equally to this work.
Acknowledgment: The authors thank the Israel Diabetes Research Group for valuable support and advice, and Dr. M.J. Stamper, Harvard School of Public Health, for valuable discussions during the early stages of this work.
Grant Support: By Ben-Gurion University of the Negev, Beer-Sheva, Israel, and funds from the Israel Defense Forces National Budget.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Iris Shai, RD, PhD, Department of Epidemiology and Health Systems Evaluation, The S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University of the Negev, PO Box 653, Beer-Sheva 84105, Israel; e-mail, firstname.lastname@example.org.
Current Author Addresses: Dr. Tirosh: Department of Internal Medicine A, Sheba Medical Center, Tel-Hashomer, Israel.
Dr. Rudich: Department of Clinical Biochemistry, The S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University of the Negev, PO Box 653, Beer-Sheva 84105, Israel.
Ms. Shochat and Drs. Tekes-Manova, Israeli, and Kochba: Medical Corps Headquarters, Israel Defense Forces, Zrifin, Israel.
Dr. Henkin: Soroka University Medical Center, Ben-Gurion University of the Negev, PO Box 653, Beer-Sheva 84105, Israel.
Dr. Shai: Department of Epidemiology and Health Systems Evaluation, The S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University of the Negev, PO Box 653, Beer-Sheva 84105, Israel.
Author Contributions: Conception and design: A. Tirosh, A. Rudich, D. Tekes-Manova, E. Israeli, I. Kochba, I. Shai.
Analysis and interpretation of the data: A. Tirosh, A. Rudich, I. Shai.
Drafting of the article: A. Tirosh, A. Rudich, I. Shai.
Critical revision of the article for important intellectual content: A. Tirosh, A. Rudich, Y. Henkin, I. Shai.
Final approval of the article: A. Tirosh, I. Shai.
Provision of study materials or patients: A. Tirosh, D. Tekes-Manova, E. Israeli, I. Kochba, I. Shai.
Statistical expertise: A. Tirosh, T. Shochat, I. Shai.
Obtaining of funding: E. Israeli.
Administrative, technical, or logistic support: D. Tekes-Manova, E. Israeli, I. Kochba.
Collection and assembly of data: T. Shochat.
Tirosh A., Rudich A., Shochat T., Tekes-Manova D., Israeli E., Henkin Y., Kochba I., Shai I.; Changes in Triglyceride Levels and Risk for Coronary Heart Disease in Young Men. Ann Intern Med. 2007;147:377-385. doi: 10.7326/0003-4819-147-6-200709180-00007
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Published: Ann Intern Med. 2007;147(6):377-385.
A recent meta-analysis (1) and most published papers suggest a moderate association between fasting triglyceride levels and coronary heart disease (CHD) (2–11). Of the lipid fractions, the triglyceride-rich very-low-density lipoprotein particle is probably the most sensitive to lifestyle modification (8). For example, estimates from meta-analyses suggest that for every 4.5 kg (approximately 10 lb) of stable weight reduction, triglyceride levels decrease by at least 0.068 mmol/L (≥6 mg/dL) (12). Accordingly, a considerable increase in the proportion of hypertriglyceridemic patients accompanies the obesity epidemic (6, 9). In addition, aerobic exercise, independent of weight loss, has been shown to modestly reduce triglyceride levels in a dose-dependent fashion (13). Hence, when assessing the risk associated with triglyceride levels, triglyceride measurement at a single time point (typically at enrollment) may not be a reliable indicator of a person's long-term triglyceridemia during follow-up. Whether changes in triglyceride levels over time can improve cardiovascular risk assessment is largely unknown, particularly in young adults, in whom information on the association between triglycerides and CHD is not available (1).
University of Arizona College of Medicine
September 27, 2007
Most important thing to be considered with an elevated triglycerides leading to coronary artery dise
Tirosh and colleagues have done an excellent observational study on relationship between triglyceride levels and risk of coronary artery disease. (1) There are few points worth mentioning "“ the sample of the population are all males and military personnel which is not representative of the population that we see in our daily clinics and wards. It is also important to note that the triglyceride levels are comparatively higher in women and diabetes; both were excluded in this study.
As already well known, that mild to moderate elevation of fasting plasma triglyceride level is common in patients with diabetes. In adult onset type diabetes, the fasting triglyceride values are highly variable but the prevalence of hypertriglyceridemia is markedly increased over that in age matched control population. Basal triglyceride level is regulated by the rate of production of circulating triglycerides and by the efficiency of their removal. In type 2 diabetes, hypertriglyceridemia results from increased plasma concentrations of VLDL, with or without chylomicronemia; deficient lipoprotein lipase activity; increased cholesteryl ester transfer protein activity; and increased flux of free fatty acids to the liver.(1)
Even though the study did not include people with diabetes; patients with high triglycerides may have sub-clinical diabetes (glucose intolerance) to start with and may have developed subsequent diabetes, putting them at risk of coronary artery disease. So I need to know whether the patients who had coronary angiogram proved CAD were investigated for the presence of diabetes or glucose intolerance at all. The increased prevalence of CAD in hypertriglyceridemia group could be because of diabetes itself playing an important role than triglycerides. As an important point life style modification, diet and exercise improves glycemic control thereby reducing the risk of CAD.
1. Tirosh A, Rudich A, Shochat T, Tekes-Manova D, Israeli E, Henkin Y, Kochba I, Shai I . Changes in Triglyceride Levels and Risk for Coronary Heart Disease in Young Men. Ann Intern Med. 2007;147(6): 377-85
2.Pollex RL, Hegele RA. Genetic determinants of the metabolic syndrome. Nat Clin Pract Cardiovasc Med 2006;3:482-9.
University of California, San Francisco
October 1, 2007
MELANY and Familial Combined Hyperlipidemia
With such a large and well-characterized study sample, is it possible to determine whether "ethnicity" contributes to either the baseline or second triglyceride level in the MELANY study? Namely, would a post-hoc analysis indicate differences among Eastern European, Central Asian, or North African Jewish subjects? Since familial combined hyperlipidemia is a prevalent, world-wide disease marked by low HDL cholesterol and hypertriglyceridemia, identifying subpopulations (and kindred) in MELANY might help unravel this nefarious disease.
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Cardiology, Dyslipidemia, Coronary Risk Factors, Coronary Heart Disease, Prevention/Screening.
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